Reply to comment on: Nrf2 regulates interferon receptor expression and alters macrophage polarization in lupus

We agree with Drs. Xu and Huang that lupus is complex. This is illustrated by lupus-like disease in mice with defective Fas (B6/lpr and MRL/lpr) vs. mice with pristane-induced lupus, which may represent distinct forms of lupus. While signaling through the type I interferon receptor (IFNAR) is implicated in pristane-induced lupus ("interferon signature"), the studies of Zhao, et al. suggest a role for IL-17 in the pathogenesis of lupus in B6/lpr mice lacking Nrf2 (Nfe2l2-/-) (1). However, lupus in lpr mice differs from lupus in pristane-treated mice and most SLE patients.